Hypermethylation at loci sensitive to the prenatal environment is associated with increased incidence of myocardial infarction
Author(s) -
Rudolf P. Talens,
J. Wouter Jukema,
Stella Trompet,
Dennis Kremer,
Rudi G. J. Westendorp,
L. H. Lumey,
Naveed Sattar,
Hein Putter,
P. Eline Slagboom,
Bastiaan T. Heijmans
Publication year - 2011
Publication title -
international journal of epidemiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.406
H-Index - 208
eISSN - 1464-3685
pISSN - 0300-5771
DOI - 10.1093/ije/dyr153
Subject(s) - dna methylation , epigenetics , odds ratio , methylation , myocardial infarction , medicine , pregnancy , genetics , endocrinology , physiology , biology , dna , gene , gene expression
Human epidemiological studies suggest that small size at birth and food deprivation during gestation confer an excess risk of coronary heart diseases (CHD) in adulthood, frequently in a sex-specific manner. Prior epigenetic studies indicate that such prenatal conditions are marked by persistent and sometimes sex-specific changes in DNA methylation. Here, we have investigated the association between DNA methylation and myocardial infarction (MI) at six loci sensitive to prenatal nutrition, anticipating potential sex-specificity. Method Within the placebo group of the PROSPER trial on pravastatin and the risk of CHD, we compared all individuals who were event free at baseline and developed MI during 3 years' follow-up (n = 122) with a similar-sized control group. Methylation at IL10, LEP, ABCA1, IGF2, INS and GNASAS was measured in DNA extracted from leucocytes using mass spectrometry.
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